The invention provides a method for the treatment of Ph+ leukemia in a patient comprising administering to the patient (i) a BCR-ABL tyrosine kinase inhibitor, and (ii) an agent which selectively binds to a cell surface receptor expressed on Ph+ leukemic stem cells. The invention further provides for the use of (i) and (ii) in, or in the manufacture of a medicament for, the treatment of Ph+ leukemia in a patient; and a composition for the treatment of Ph+ leukemia in a patient comprising (i) and (ii); and kits comprising (i) and (ii). In some embodiments, the tyrosine kinase inhibitor is or is not imatinib; or is selected from the group consisting of dasatinib, nilotinib, bosutinib, axitinib, cediranib, crizotinib, damnacanthal, gefitinib, lapatinib, lestaurtinib, neratinib, semaxanib, sunitinib, toceranib, tyrphostins, vandetanib, vatalanib, INNO-406, AP24534, XL228, PHA-739358, MK-0457, SGX393 and DC2036; or is selected from the group consisting of dasatinib and nilotinib. In some embodiments, the agent binds to a receptor involved in signalling by at least one of IL-3, G-CSF and GM-CSF. In some embodiments, the agent is a mutein selected from the group consisting of IL-3 muteins, G-CSF muteins and GM-CSF muteins. In some embodiments, the mutein is an IL-3 mutein. In some embodiments, the agent is a soluble receptor which is capable of binding to IL-3.

The present disclosure provides a method for treating lupus, Sjörgen's syndrome or scleroderma, the method comprising administering to the mammal an immunoglobulin which binds an interleukin 3 receptor α (IL-3Rα) chain and which depletes or at least partly eliminates plasmacytoid dendritic cells (p DCs) and basophils to which it binds.

The present invention provides methods for inhibiting interleukin-3 receptor-expressing cells, and, in particular, inhibiting the growth of such cells by using a diphtheria toxin-human interleukin-3 conjugate (DT-IL3) that is toxic to cells expressing the interleukin-3 receptor. In preferred embodiments, the DT-IL3 conjugate is a fusion protein comprising amino acids 1-388 of diphtheria toxin fused via a peptide linker to full-length, human interleukin-3. In certain embodiments, the methods of the present invention relate to the administration of a DT-IL3 conjugate to inhibit the growth of cancer cells and/or cancer stem cells in humans, which cells express one or more subunits of the interleukin-3 receptor. Exemplary cells include myeloid leukemia cancer stem cells. In other embodiments, the methods of the present invention relate to ex vivo purging of bone marrow or peripheral blood to remove cells that express one or more subunits of the interleukin-3 receptor such that the purged bone marrow or peripheral blood is suitable, e.g., for autologous stem cell transplantation to restore hematopoietic function.

The present invention provides methods for inhibiting interleukin-3 receptor-expressing cells, and, in particular, inhibiting the growth of such cells by using a diphtheria toxin-human interleukin-3 conjugate (DT-IL3) that is toxic to cells expressing the interleukin-3 receptor. In preferred embodiments, the DT-IL3 conjugate is a fusion protein comprising amino acids 1-388 of diphtheria toxin fused via a peptide linker to full-length, human interleukin-3. In certain embodiments, the methods of the present invention relate to the administration of a DT-IL3 conjugate to inhibit the growth of cancer cells and/or cancer stem cells in humans, which cells express one or more subunits of the interleukin-3 receptor. Exemplary cells include myeloid leukemia cancer stem cells. In other embodiments, the methods of the present invention relate to ex vivo purging of bone marrow or peripheral blood to remove cells that express one or more subunits of the interleukin-3 receptor such that the purged bone marrow or peripheral blood is suitable, e.g., for autologous stem cell transplantation to restore hematopoietic function.

The present disclosure provides, in part, a method of treating an autoimmune disease in a subject by reducing the number of pDCs through administration of a human interleukin-3 (IL-3)-diphtheria toxin conjugate (DT-IL3). The disclosure also generally relates to methods of monitoring the effectiveness of therapy in subjects receiving DT-IL3 for treating an autoimmune disease, and methods of determining continuing treatment of subjects receiving DT-IL3 for treating an autoimmune disease. The disclosure also provides pharmaceutical compositions of DT-IL3 for use in such methods.

The invention relates to the combined use of selective serotonin reuptake inhibitors (SSRIs) and hematopoietic growth factors as a drug and particularly for treating cytopenia related to hematopoietic diseases or chemotherapy, and also to a pharmaceutical kit comprising both SSRIs and hematopoietic growth factors. This combination is more particularly used for treating patients presenting cytopenia, and patients in need of chemotherapy and more particularly to reduce length of chemotherapy-induced aplasia.

The invention relates to the combined use of selective serotonin reuptake inhibitors (SSRIs) and hematopoietic growth factors as a drug and particularly for treating cytopenia related to hematopoietic diseases or chemotherapy, and also to a pharmaceutical kit comprising both SSRIs and hematopoietic growth factors. This combination is more particularly used for treating patients presenting cytopenia, and patients in need of chemotherapy and more particularly to reduce length of chemotherapy-induced aplasia.

The present invention provides methods for treating or inhibiting a myeloproliferative neoplasm (MPN) in a subject in need thereof, comprising administering to the subject a diphtheria toxin-human interleukin-3 conjugate (DT-IL3) and one or more Jak inhibitors and/or one or more hypomethylating agents.

The present invention provides methods for treating or inhibiting a myeloproliferative neoplasm (MPN) in a subject in need thereof, comprising administering to the subject a diphtheria toxin-human interleukin-3 conjugate (DT-IL3) and one or more Jak inhibitors and/or one or more hypomethylating agents.

Provided herein are improved formulations of tagraxofusp for lyophilization used to manufacture stable formulations of tagraxofusp for intravenous injection.